0572 High Residual Apnea Burden may Contribute to Frequent Outcome Failure in Randomized Controlled Trials of Positive Airway Pressure - a Proof-of-Concept Study

Background: Bi-level noninvasive ventilation (NIV) has been used in respiratory distress syndrome (RDS) as primary treatment, post-extubation, and to treat apnea. This review summarizes studies on bi-level NIV in premature infants with RDS. Nonsynchronized nasal intermittent positive pressure ventilation (nsNIPPV) and synchronized NIPPV (SNIPPV) use pressure settings ≥ those used during mechanical ventilation (MV), and biphasic continuous positive airway pressure (BiPAP) use two nasal continuous positive airway pressure (NCPAP) levels ≤4 cm H2O apart. Methods: A systematic review (Medline OVID and Pubmed) and meta-analysis of randomized controlled trials. Primary outcomes were bronchopulmonary dysplasia (BPD) and mortality. Secondary outcomes included NIV failure (intubation) and extubation failure (re-intubation). Data were pooled using a fixed-effects model to calculate the relative risk (RR) with 95% confidence interval (CI) between NIV modes (RevMan v 5.3, Copenhagen, Denmark). Results: Twenty-four randomized controlled trials that largely did not correct for mean airway pressure (MAP) and used outdated ventilators were included. Compared with NCPAP, both nsNIPPV and SNIPPV resulted in less re-intubation (RR 0.88 with 95% CI (0.80, 0.97) and RR 0.20 (0.10, 0.38), respectively) and BPD (RR 0.69 (0.49, 0.97) and RR 0.51 (0.29, 0.88), respectively). nsNIPPV also resulted in less intubation (RR 0.57 (0.45, 0.73) versus NCPAP, with no difference in mortality. One study showed less intubation in BiPAP versus NCPAP. Conclusions: Bi-level NIV versus NCPAP may reduce MV and BPD in premature infants with RDS. Studies comparing equivalent MAP utilizing currently available machines are needed.

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Obstructive Sleep Apnea–Induced Neurogenic Nocturnal Hypertension

Hypertension ◽

10.1161/hypertensionaha.120.16378 ◽

2021 ◽

Author(s):

Kazuomi Kario ◽

Douglas A. Hettrick ◽

Aleksander Prejbisz ◽

Andrzej Januszewicz

Keyword(s):

Blood Pressure ◽

Obstructive Sleep Apnea ◽

Continuous Positive Airway Pressure ◽

Airway Pressure ◽

Renal Denervation ◽

Positive Airway Pressure ◽

Controlled Trials ◽

Nocturnal Hypertension ◽

Randomized Controlled ◽

Obstructive Sleep

There is a bidirectional, causal relationship between obstructive sleep apnea (OSA) and hypertension. OSA-related hypertension is characterized by high rates of masked hypertension, elevated nighttime blood pressure, a nondipper pattern of nocturnal hypertension, and abnormal blood pressure variability. Hypoxia/hypercapnia-related sympathetic activation is a key pathophysiological mechanism linking the 2 conditions. Intermittent hypoxia also stimulates the renin-angiotensin-aldosterone system to promote hypertension development. The negative and additive cardiovascular effects of OSA and hypertension highlight the importance of effectively managing these conditions, especially when they coexist in the same patient. Continuous positive airway pressure is the gold standard therapy for OSA but its effects on blood pressure are relatively modest. Furthermore, this treatment did not reduce the cardiovascular event rate in nonsleepy patients with OSA in randomized controlled trials. Antihypertensive agents targeting sympathetic pathways or the renin-angiotensin-aldosterone system have theoretical potential in comorbid hypertension and OSA, but current evidence is limited and combination strategies are often required in drug resistant or refractory patients. The key role of sympathetic nervous system activation in the development of hypertension in OSA suggests potential for catheter-based renal sympathetic denervation. Although long-term, randomized controlled trials are needed, available data indicate sustained and relevant reductions in blood pressure in patients with hypertension and OSA after renal denervation, with the potential to also improve respiratory parameters. The combination of lifestyle interventions, optimal pharmacological therapy, continuous positive airway pressure therapy, and perhaps also renal denervation might improve cardiovascular risk in patients with OSA.

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